This research was supported in part by grants to J.F.S. from the National Institute of Mental Health (RO1-MH46801 & T32-MH18831), the National Institute on Aging (PO1-AG11585), and the John D. and Catherine T. MacArthur Foundation.
Stress-Induced Neuroendocrine Modulation of Viral Pathogenesis and Immunitya
Article first published online: 7 FEB 2006
Annals of the New York Academy of Sciences
Volume 840, NEUROIMMUNOMODULATION: MOLECULAR ASPECTS, INTEGRATIVE SYSTEMS, AND CLINICAL ADVANCES pages 803–808, May 1998
How to Cite
SHERIDAN, J. F., DOBBS, C., JUNG, J., CHU, X., KONSTANTINOS, A., PADGETT, D. and GLASER, R. (1998), Stress-Induced Neuroendocrine Modulation of Viral Pathogenesis and Immunity. Annals of the New York Academy of Sciences, 840: 803–808. doi: 10.1111/j.1749-6632.1998.tb09618.x
- Issue published online: 7 FEB 2006
- Article first published online: 7 FEB 2006
Abstract: Physical restraint (RST) was used to examine the interactions among the hypothalamic-pituitary-adrenal (HPA) axis, sympathetic nervous system, and the immune response to infection. In these studies, mice were infected with either herpes simplex virus (HSV) or influenza A/PR8 virus so that the impact of neuroendocrine activation could be assessed on disease pathophysiology and anti-viral immunity. RST suppressed lymphadenopathy in draining lymph nodes, reduced mononuclear cellular infiltration in the lungs, and suppressed virus-specific cytokine and cytolytic T-cell responses. Blockade of type II glucocorticoid receptors (by RU486) restored cellularity and cytokine responses to both organs in restraint-stressed, infected mice. Thus, the HPA axis modulated cell trafficking and T-cell cytokine responses. However, RU486 treatment failed to restore cytolytic T-cell responses. Blockade of β-adrenergic receptors (by nadolol), in combination with RU486 treatment, fully restored cytolytic T-cell responses, suggesting that catecholamines were involved in suppressing the virus-specific CD8+ cytolytic T-cell response. RST also modulated the local development or expression of antibody-secreting cells (ASC) in the lungs draining lymph nodes, and spleen following infection of restrained mice. RST significantly suppressed the number of virus-specific ASC (IgM, IgG and subclasses IgG1 and IgG2a) in the lungs, mediastinal (MLN) lymph nodes and spleen, while it enhanced the responses in the superficial cervical (SCV) lymph nodes. This observation of differential modulation of ASC responses in the MLN and SCV lymph nodes supports the concept of tissue-specific immunoregulation in response to stress.